Linked Life Data

6106025

Source:http://linkedlifedata.com/resource/pubmed/id/6106025

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1980-11-24
pubmed:abstractText
Methoxamine and phenylephrine (PE), postsynaptic alpha adrenergic agonists stimulated the accumulation of cyclic AMP in spinal cord tissue slices. Naphazoline, oxymetazoline and clonidine, previously shown to have greater efficacy at presynaptic alpha receptors did not alter accumulation and, in fact, blocked the PE response. The PE-stimulation was completely inhibited by postsynaptic alpha antagonists, incompletely by agents which bl ock presynaptic alpha receptors, and slightly by the beta blocker propranolol. Pe-stimulated accumulation was potentiated by phosphodiesterase inhibition (RO 20-1724). In contrast to previous reports on the requirement of the copresence of adenosine for alpha receptor stimulated accumulation of cyclic AMP in neuronal tissue, the PE-stimulation in spinal cord slices was unchanged by adenosine receptor blockade (theophylline), hydrolysis of endogenous adenosine (adenosine deaminase), inhibition of adenosine deaminase (EHNA) or blockade of adenosine uptake (dipyridamole). Added adenosine increased basal accumulation and produced a marked potentiation of the PE response. From this data it is evident that, in spinal cord tissue slices, there occurs a postsynaptic alpha adrenergic receptor linked to cyclic AMP accumulation which does not require the presence of other neurohumoral agents for activation.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0095-1544
pubmed:author
pubmed:issnType
Print
pubmed:volume
6
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
133-41
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1980
pubmed:articleTitle
Alpha adrenergic receptor mediated formation of cyclic AMP in rat spinal cord.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.